Removal of iatrogenic orbital foreign bodies with a 3D model.

Facial foreign body (FB) is common after trauma, but iatrogenic orbital FB is a rare and unexpected complication of facial FB removal surgery. We present the case of a 43-year-old man with a glass FB in his nose. During the operation, this FB broke into two pieces, and the larger one pierced into the left orbit, close to the eyeball. A three-dimensional (3D) model was made that accurately recreated the shape and position of the FB in the orbit, according to which the FB was removed. 3D-printing technology is a great tool when dealing with complex facial FB.

Remodeled structure and reduced contractile responsiveness of ocular ciliary artery in spontaneously hypertensive rats.

AIM: To investigate the alterations in both structure and contractile responsiveness of ocular ciliary artery (OCA) in spontaneously hypertensive rat (SHR). METHODS: In this experiment, 20-week-old male SHR and Wistar Kyoto rat (WKY) were studied. The heart rate (HR), the blood pressure (BP; the systolic BP and the diastolic BP) of rats with an electronic sphygmomanometer were measured. Vascular morphometry and isometric tension measurement were used to investigate the alterations in structure and contractility of OCA. RESULTS: A general narrowing of OCAs was observed in SHR compared to the control WYK. In SHR, the media of OCAs were thicker, the luminal diameters were smaller, and the media-to-lumen ratios were higher when compared with WKY (P<0.05). The contractions of OCAs evoked by norepinephrine were smaller in SHR compared to control (P<0.05). Then, OCAs were pretreated with iberiotoxin, L-NAME, or indomethacin 30min before norepinephrine-induced contraction. Iberiotoxin (0.1 µmol/L) has not changed the norepinephrine-induced contractions in OCAs from both groups. However, L-NAME (100 µmol/L) increased the vasoconstrictions, the increased extents were similar in SHR and WKY (P>0.05). Indomethacin (10 µmol/L) decreased the contractions induced by norepinephrine in OCAs from WKY (P<0.05), but did not change those contractions in vessels from SHR (P>0.05). CONCLUSION: Our results demonstrate that the structure and function of OCAs are altered in hypertension. OCAs from SHR are remodeled with decreased lumen diameter and increased media-to-lumen ratio. Moreover, the contractile responsiveness of OCAs from SHR is diminished due to the disruption of vasoconstrictive effect of prostaglandins.

Effects of brinzolamide on rabbit ocular blood flow in vivo and ex vivo.

AIM: To investigate if significant improvement of optic disc blood flow (ODBF) occurs after instillation of brinzolamide onto rabbit eyes. METHODS: Testing of bilateral intraocular pressure (IOP) and left ODBF in 10 male rabbits took place every 3h over a 24h period. Brinzolamide (1% ophthalmic solution, two drops at 9:00 and 21:00) was administered to the left eye. ODBF, assessed using laser speckle flowgraphy, was determined as the mean blur rate (MBR). Furthermore, the effect of brinzolamide on isolated rabbit ciliary arteries using isometric tension recording system was performed. RESULTS: After brinzolamide instillation, IOP was significantly decreased in the left eye. MBR-vessel was greater at 18:00 and 21:00 (P<0.05) than in the controls. MBR-tissue and MBR-average were greater at 18:00 (P<0.05) than in the controls. For isolated arteries pre-contracted with a high-K solution, brinzolamide induced concentration-dependent relaxation, reaching 46.1%±9% (n=21) at 1 mmol/L. In Ca2+-free solutions, incubation with brinzolamide suppressed 1 µmol/L histamine-induced contractions (P<0.05). CONCLUSION: Brinzolamide decreases IOP and increases ocular blood flow. The direct vasodilatory effect of brizolamide is mediated by suppression of Ca2+ release from intracellular calcium stores.

Microstructure, friction and corrosion resistance properties of a Ni-Co-Al2O3 composite coating.

Ni-Co-Al2O3 composite coatings were prepared by pulsed electrodeposition and electrophoresis-electrodeposition on aluminum alloy. The content of Al2O3 particles of the Ni-Co-Al2O3 composite coating prepared by electrophoresis-electrodeposition was significantly higher than the composite coating prepared by pulsed electrodeposition. The composite coating prepared by electrophoresis-electrodeposition exhibited a better anti-wear performance than that prepared by pulsed electrodeposition. The morphology, composition and microstructure of the composite coatings were determined by means of X-ray diffractometer (XRD) and scanning electron microscopy (SEM). The hardness and friction properties of the samples were tested on the microhardness tester and the friction and wear loss tester respectively.

Antimicrobial and antioxidant activities of Flammulina velutipes polysaccharides and polysaccharide-iron(III) complex [corrected].

FVP is polysacchrides obtained from Flammulina velutipes. A polysacchride named FVP2 was isolated from FVP by DEAE cellulose-52 chromatography and Sephadex G-100 size-exclusion chromatography. FVP-Fe and FVP2-Fe were synthesized by neutralization of FeCl3 carbohydrate solution. The antibacterial and antifungal activities of FVP, FVP2, FVP-Fe, FVP2-Fe were investigated and their antioxidant effects on hydroxyl, 2,2-diphenyl-1-picrylhydrazyl (DPPH), superoxide anion, 2,2'-azobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radicals, reducing power, inhibition of malondialdehyde (MDA) were assessed in vitro. The results suggested that FVP-Fe and FVP2-Fe significantly suppressed the growth of bacteria Staphylococcus aureus, Escherichia coli, and Bacillus subtilis, and have relatively strong antioxidant activity to scavenge superoxide anion radical. In addition, FVP exhibited strong antioxidant activity to eliminate hydroxyl, DPPH, ABTS radicals, had high reducing power and inhibited the MDA production of health mice liver homogenate induced by auto-oxidation and Fe2+-H2O2 system.

Angiotensin II type 1 receptor blockade suppresses H2O2-induced retinal degeneration in photoreceptor cells.

Exposure to reactive oxygen species (ROS) leads to the development and progression of retinal degenerative diseases. However, the exact mechanisms are not fully understood. In this article, the role of angiotensin II type 1 receptor (AT1R) signaling in H(2)O(2)-induced retinal damage was examined. Mouse photoreceptor-derived 661 W cells were treated with the AT1R blockers valsartan, losartan and candesartan before exposure to H(2)O(2). Cell viability, intracellular ROS level, mitochondrial membrane potential (MMP), cytochrome-c level, DNA fragmentation, caspase activity and gene expression were detected. Pre-treatment of 661 W cells with AT1R blockers significantly decreased H(2)O(2)-mediated toxicity and reduced the ROS level. In addition, apoptosis-related biochemical indicators showed that pre-incubation of AT1R blockers would elevate the MMP, decrease the release of cytochrome-c and formation of DNA fragmentation, and inhibit activities of caspase-3 and caspase-9 in exogenous H(2)O(2)-treated 661 W cells. Moreover, treatment with AT1R blockers suppressed the expression of Egr1, Fosl1 and Lox12. These results suggest that AT1R signaling mediates H(2)O(2)-induced apoptosis, at least partially through generating the ROS and increasing the levels of proapoptotic molecules in 661 W cells. AT1R blockade may provide a new therapeutic approach for preventing oxidative stress-induced retinal neural damage.